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The Brain Electrical Activity Mapping (BEAM) of Vestibular Evoked Potentials (VestEP) is a new method in the toolbox of the neurootologist.
The aim of following two case presentations is to demonstrate the method of cortical Vestibular Evoked Potentials (VestEP) displayed by its combination with Brain Electrical Activity Mapping (BEAM).1 The VestEP-BEAM method provides reliable clinical information about the functional state of the vestibular endorgan, its brain stem pathways and cortical representation. A 47-year-old male was referred in 1995 to the Neurootology department with a presumed diagnosis of total bilateral vestibular loss.
1980 - Right otitis herpetica with right facial palsy and the complication of encephalitis herpetica with resultant progressive severe hearing and vestibular loss right.
Absent potentials for the left ear and pathological morphology of the curves, with prolonged interpeak latency of the waves III-V for the right ear.
These could be cognitive potentials due to proprioceptive stimuli, coming from cervical and body receptors. A 57-year-old male was referred to our department in September 1995 for neurootologic investigation, for a presumed diagnoses of complete bilateral vestibular loss and suspicion of right acoustic neurinoma. Delayed acoustic brain stem evoked potentials, to the level of the Colliculus inferior, bilaterally, with either left and right stimulation.
Normal image of cerebello-pontine angle, meatus acousticus intern us, VIIIth cranial nerve, cochlea, and semicircular canals. We recommended therapy with Betahistine (Vasomotal®) 8 mg x 3 times daily and a follow-up examination after three months. The patient returned after three months of therapy with unchanged bilateral tinnitus and reported a slight amelioration of the hearing, which was objectified with audiometric testing (10dB at the right ear, 5 dB at the left ear).
Central (probably mesencephalic) vestibular affection, with inhibition of the nystagmus generator centers.Bilateral affection of the acoustical receptors and probably of the brain stem acoustical pathways.
The patient was recommended to continue therapy with Betahistine, and to make supplementary cardiovascular and blood tests (coagulation study, serum cholesterol and triglyceride etc). In the first case, where the symptomatology is dominated by the severe disequilibrium complaints, this diagnosis is confirmed by the VestEP-BEAM investigation.
In the second case, any symptoms suggesting an affection of the vestibular system are absent. We thank Christo Kolchev, MD, Neurologist, for his excellent scientific discussions and advice.
The aim of our study was to outline the prevalence of hyperlipidemia in patients who had high-frequency hearing loss and tinnitus due to noise exposure. Cochlear hair cells and neural and central auditory pathways are involved in the generation of subjective tinnitus [1]. Decrease in internal diameter of the vascular bed resulting from hyperlipidemia compromises the oxygen transportation capability of the blood to the cochlea, and chronic hypoxia is likely to occur by the reduction in oxygen supply of the inner ear, which in turn would lead to insufficient adjustment of the cochlear metabolism. This may result in the overproduction and accumulation of free radicals, which disturb the microcirculation of the cochlea and play an important role in ischemiainduced cochlear injury [7]. The reasons for the susceptibility to noise-induced hearing loss of patients who have been exposed to a noisy environment have been the subject of various studies. Previous data indicate that the cochlea and the central auditory system age faster and earlier in patients with hyperlipidemia and that the risk of noise-induced hearing loss is much higher [5,11]. The aim of this study was to outline the prevalence of hyperlipidemia in patients who had high-frequency hearing loss and tinnitus due to chronic noise exposure and to evaluate the risk of developing sensory hearing loss in those patients as compared to risk in control subjects. We conducted this prospective study in 120 consecutive patients with complaints of chronic subjective tinnitus of varying degrees of severity and hearing loss due to noise exposure. The patients were examined otoscopically and were reviewed by an audiometric test battery including puretone audiometer (AC-30, IAC, Copenhagen, Denmark), stapes reflex, and tympanometry (Amplaid 775, Milan, Italy).
Antilipid treatment with statin derivatives was planned once-daily oral dosing for up to 1-2 years (minimum, 12.4 months).
We then compared tinnitus scores and hearing levels in patients with no response to antihyperlipidemic therapy and in patients who had a normal blood cholesterol level after the treatment.
The duration of tinnitus in patients with noise exposure varied from 2 months to 12 years (mean, 5.5 years). Of 22 patients in the unresponsive group, 6 had high cholesterol and triglyceride, 9 had high triglyceride, and 7 had high cholesterol only before the antilipidemic therapy.
Of 20 patients in the responsive group, 7 had high cholesterol or triglyceride, 10 had high triglyceride, and 3 had high cholesterol only before the antilipidemic therapy. The difference between the pitch-match frequencies before and after therapy was not significant. Epidemiological investigations emphasizing the relationship between hearing loss and the risk factors for coronary artery disease date back to the 1960s [18]. Spencer [19] found that 42.3% of 300 patients with different symptoms of inner-ear pathology had clearly defined hyperlipoproteinemia. The effect of hyperlipidemia on auditory perception has been studied clinically and experimentally. The exact pathological mechanism for the hyperlipidemia-induced hearing loss remains obscure. In his study of 64 rats, Pillsbury [37] exposed half to loud noise and fed half of each subgroup a fat diet and found elevated auditory brainstem response thresholds in the hyperlipidemic animals. Studies investigating the restorative possibility of a low-cholesterol diet and antihyperlipidemic therapy on hearing loss and tinnitus are very few. LDL apheresis has been reported to be much more effective as compared with standard prednisolone, dextran, and pentoxifylline therapy in patients with sudden hearing loss [9]. In our study, changes in tinnitus scores before and after therapy in the responsive group were significant as compared with those in the unresponsive group. Tinnitus and hearing loss are frequently encountered after an acute acoustic and blast trauma or chronic noise exposure. Stapedectomy: involves removing a portion of the adherent stapes and replacing it with an implant. Microdrill and CO2 laser Stapedotomy: this involving making a hole in the stapes footplate and inserting a piston-like prosthesis.
A 25-year-old man presents with progressive bilateral hearing loss, tinnitus, and neck pain. Two cases of bilateral vestibular loss, diagnosed by classical neurootological methods (highlighted by caloric and optokinetic tests' electronystagmography recording), are reported.
A total of 25 acceleration steps are applied for each clockwise (CW) and counterclockwise (CCW) rotations.
The patient was not able to perform more than 30 steps during Unterberger test (normal=100) and to keep standing more than 27 seconds (normal=60 sec.) in Romberg test. 3A and 3B) However, very small and hardly detectable responses with latencies of about 330 msec. His neurootological complaints were subjective bilateral tinnitus of Tinnitus cranii sive cerebri type, and a sudden aggravation of the bilateral high frequency hearing loss. Case 2 - CCO recording: pathological right deviation in the stepping test (mirrored image).

7 A and B show, VestEP elicited by either CWor CCW-rotations are markedly pathological: abnormal configuration of the waves, low voltage amplitudes. Bilateral affection ofthe peripheral acoustical organs and probably of the brain stem acoustical pathways.
The potentials were better detectable in all the examined derivations; the waves had higher amplitudes and significantly better morphologies. The sine qua non condition for the generation of normal Vestibular Evoked Potentials is the morpho-functional integrity of the vestibular system, including receptors, brain stem pathways and cortical centers. Claussen C-F, Schneider D, Marcondes LG, Patil N: A Computer Analysis of Typical CCG Patterns in 1021 Neurootological Patients. Kolchev Ch, Claussen C-F, Schneider D, Constantinescu L, Carducci F, Sandris W: Extended Normative Data on VestEP displayed by BEAM. Kolchev Ch, Claussen C-F, Schneider D: Vestibular Evoked Potentials in Central Vertigo Cases. Claussen C-F, Schneider D, Kolchev Ch: On the functional State of Central Vestibular Structures in Monaural Symptomatic Tinnitus Patients.
Low-Cholesterol Diet and Antilipid Therapy in Managing Tinnitus and Hearing Loss in Patients with Noise-Induced Hearing Loss and Hyperlipidemia. We investigated the role of a low-cholesterol diet and antihyperlipidemic therapy to alleviate the severity of tinnitus and possibly promote hearing gain after therapy in patients with acoustic trauma. Analysis of the epidemiological data indicates that exposure to noise is widespread and is one of the most common causes of tinnitus, which leads to various somatic and psychological disorders and interferes with the quality of life [2]. Auditory perception in such cochleas is very sensitive to reduction of the oxygenation in the inner ear [6]. Platelet aggregation and blood viscosity due to high lipid levels will intensify inner-ear damage owing to slowing of microcirculation and will contribute to the development of both progressive and sudden hearing loss [8,9]. Gratton and Wright [10] demonstrated the accumulation of lipid in the stria vascularis and outer hair cells in chinchillas after experimentally induced hypercholesterolemia, which might intensify the detrimental effect of ototoxic drugs or noise. We instituted a low-cholesterol diet and antihyperlipidemic therapy to investigate whether any benefit accrued in terms of hearing gain and tinnitus relief.
The project was approved by the local medical research ethical committee, and we obtained informed consent from each patient. Audiometric tests included air- and boneconduction thresholds for pure tones of 125-8,000 Hz, tests of speech reception and speech discrimination, contralateral and ipsilateral reflex measurements, and tympanometry.
Measurement of loudness of the tinnitus was based on subjective assessment by the patients. Daily dosage ranged from 10 to 40 mg for simvastatin (Zocor) and from 10 to 80 mg for atorvastatin calcium (Lipitor). Average ages of patients in the unresponsive and the responsive groups were 39 and 42 years, respectively. Wilcoxon and Mann-Whitney U tests were used to compare the pretreatment data with the posttreatment results and to compare the results of responders and nonresponders. None of these patients demonstrated any drop to normal ranges in cholesterol or triglyceride values after the treatment. When those patients were asked to qualify the severity of their tinnitus, seven rated their tinnitus as the same (35%), two rated it as increased (10%), seven rated it as decreased (35%), and four had no tinnitus (20%). The correlation between serum lipids and auditory dysfunction has been investigated before, and it has been reported that sensorineural hearing loss is more prominent in those with high levels of cholesterol, triglyceride, and lowLDL and in patients with low HDL concentration [18-23]. Increased blood viscosity and atherosclerosis of the cochlear vessels reduce the blood perfusion of the cochlea and promote hearing impairment [6,8,19,20,23,24]. When patients were required to qualify the severity of their tinnitus, 35% of the patients in the responsive group rated their tinnitus as decreased, and 20% of patients reported no tinnitus. Even though other factors making the patients susceptible to noise-induced hearing loss should be considered, on the basis of present results it can be concluded that the incidence of hyperlipidemia is high among patients with noise-induced hearing loss and that significant improvement in lowered intensity of tinnitus and in average hearing thresholds at higher frequencies can be achieved after lowering patients' serum lipid level [43]. However, otosclerosis can also affect the bony aspect of the cochlea and its nerve cells causing sensorineural hearing loss. The additional information, provided by the Vestibular Evoked Potentials (VestEP) and its high clinical significance for a more accurate neurootologic diagnosis are discussed.
The history of his disease began in 1963, with the diagnosis of a complete cochleovestibular loss left, due to a Jaffe-Lichtenstein Syndrome (fibrose bone dystrophy with secondary cysts formation at left petrous bone, mastoid process, and occipital squama). The severity of these complaints was relatively mild at onset in 1989, but then it increased progressively. The latencies of the main components, and especially of wave III are normal in CW-rotation, but significantly shortened (25 msec.) in CCW-rotation. We found extremely interesting the manner in which the complete absence of the vestibular function, as well as the very severe affection of the auditory function, were compensated by the visual and proprioceptive functions, the patient being able to lead a relatively normal life, with a satisfactory degree of social independency.
This case is more complex and thanks to the information supplied by the VestEP-BEAM method, we could make some suppositions about the location and the mechanisms of the neurootological disorders and recommend a correct therapy.
Fortytwo hyperlipidemic patients with subjective tinnitus and hearing loss due to noise exposure were enrolled for the study. It has been reported that high-plasma cholesterol and triglyceride levels are one of the major risk factors for the development of occupational hearing loss [3-5]. It seems that noise and other metabolic disturbances have a synergistic effect on the development of tinnitus and hearing loss [5]. A diagnosis of acoustic trauma was verified by an ear, nose, and throat physician according to a clinical history of chronic noise exposure in patients who sought medical help for complaints of tinnitus and high-frequency hearing loss. Patients who had chronic otitis media or middle-ear effusion, those with an abnormal ear drum (perforation, retraction, etc.) or auditory canal, and those who had abnormal tympanometry (other than type A) were excluded. In the study, from 120 patients we chose 42 male patients (35%) with elevated cholesterol or triglyceride or both (age range, 19-60 years; mean age, 45 years).
The patients were separated into two groups: the "unresponsive" group, made up of 22 patients who had no response to either of the therapies and still had hyperlipidemia, and the "responsive" group, consisting of 20 patients who had lower cholesterol or triglyceride levels. The results of the blood lipid profiles were withheld from the individual to prevent a placebo effect with the tinnitus therapy.
The significance of the difference in patient's comments on their tinnitus after the treatment ("same," "decreased," "increased," and "disappeared") was analyzed using McNemar and chi-square tests. However, the incidence of hyperlipidemia among a selected group of patients with neurosensory hearing loss varies.
They selected a group of subjects aged between 20 and 50 years and compared auditory thresholds at high frequencies and serum lipid levels.
Noise and metabolic disturbances have a synergistic effect on the development of tinnitus and hearing loss.
Effects of experimental cochlear thrombosis on oxygenation: Auditory function of the inner ear.
Direct effects of intraperilymphatic reactive oxygen species generation on cochlear function.
Clinical utility of LDL-apheresis in the treatment of sudden hearing loss: A prospective, randomized study.

The relation of hearing in the elderly to the presence of cardiovascular disease and cardiovascular risk factors. Appearance of free radicals in the guinea pig inner ear after noise-induced acoustic trauma. Progressive sensorineural hearing loss, subjective tinnitus and vertigo caused by elevated blood lipids.
A comparison of auditory brainstem evoked potentials in hyperlipidemic and normolipidemic subjects. Exploration of the early auditory effects of hyperlipoproteinemia and diabetes mellitus using otoacoustic emissions. Hypertension, hyperlipoproteinemia, chronic noise exposure: Is there a synergism in cochlear pathology? Effects of noise exposure and hypercholesterolemia on auditory function in the New Zealand white rabbit. Hearing improvement after therapy for hyperlipidemia in patients with chronic-phase sudden deafness. A prospective case-controlled study of 197 men, 50-60 years old, selected at random from a population at risk from hyperlipidemia to examine the relationship between hyperlipidemia and sensorineural hearing loss. Jaffe-Lichtenstein Syndrome affecting left petrous bone, mastoid process, and occipital squama: A. Since 1985, the patient also complained of sinoatrial bradycardia and tendency to low blood pressure. 10A and B) There was also a tendency to normalization of the latencies, especially of the wave III, in the CCW-rotation (15 msec.
The more severe and extended the lesions are, the more disturbed will be the recorded VestEP.
Thus, the results of the complete neurootological examination demonstrate that both the acoustic and vestibular systems are affected by the pathological process.
All patients who were required to complete the questionnaire and who were subjected to clinical examination were military personnel. A pure-tone signal was presented continuously at 50-Hz intervals at between 10- and 20-dB levels. We placed all these patients on a low-cholesterol diet or antihyperlipidemic therapy (Table 2). When patients were asked to qualify the severity of their tinnitus, 10 rated their tinnitus as the same (47%), 9 rated it as increased (42%), 2 rated it as decreased (9%), and 1 patient had no tinnitus (2%).
Lowry and Isaacson [12] reported 20% hyperlipoproteinemia among 100 patients with bilateral hearing loss.
Lipidosis of the inner ear has been postulated by Nguyen and Brownell [33] as an alternate mechanism.
Insufficient perfusion of the cochlea due to increased blood viscosity and microthrombosis related to hyperlipidemia has been claimed to cause susceptibility to noiseinduced hearing loss [35].
We found in our study that the incidence of hyperlipidemia among patients with noiseinduced tinnitus and hearing loss was 35%. Characteristics of tinnitus and etiology of associated hearing loss: A study of 123 patients. The most active areas (dark yellow), corresponding to the suspected electrical events with latencies of about 330 msec., have a frontal distribution.
We excluded on the basis of their response to the questionnaire or clinical examination subjects who had a history of familial hearing loss, head trauma, collagen disease, neurological or hormonal disturbance, addiction to alcohol, or ototoxic drug therapy. The main criteria for response to the antihyperlipidemic therapy was defined as a return to normal cholesterol or triglyceride levels after therapy or at least a 40% drop from either of the initial blood cholesterol or triglyceride levels if the values were slightly above the normal limits. The latter authors showed that the lateral wall of outer hair cells from guinea pig cochlea incorporates water-soluble cholesterol.
Axelsson and Lindgren [34] matched 78 men at age 50 years with high serum cholesterol levels to 75 randomly selected 50-year-old men and found significant correlation between noise exposure and high cholesterol level. Therefore we can speak about a combined acoustic and vestibular, peripheral and central neurootological syndrome. The difference between tinnitus scores in the unresponsive and responsive groups and the change in tinnitus scores before and after therapy in the responsive group were significant. None of the patients had cerebrovascular disease, hypertension, electrolyte imbalance, cranial nerve deficit, or clinical signs of peripheral neuropathy.
Then, the pitch-match frequency threshold of the tinnitus was measured as the tinnitus loudness match of the pure-tone stimulus presented with a 1-dB increase of tinnitus frequency. Morizono and Paparella [30], using cholesterolfed rabbits, showed increased auditory dysfunction with time at all frequencies. This uptake of cholesterol is accompanied by an increased stiffness of the cells, which may impair the cells' electromotile response. Enhancement of cochlear action potentials and auditory brainstem responses has been demonstrated after limited intake of cholesterol. However, patients were at the chronic phase, more than 1 month from the onset of the hearing loss.
It most likely reflects a vascular insufficiency within the vertebro-basilar system due to possible micro-tromboembolization, rheological changes, dynamic circulatory insufficiency, more pronounced on the left side. It seems that the order of destruction and the high-frequency nature of the auditory dysfunction are correlated not only with the frequency and severity of the noise exposure but with the presence of the secondary pathology, as the formation of vasoactive lipid peroxidation products after intense noise is similar to the condition seen in metabolic damage to the organ of Corti [7,14-17]. In a survey of 44 patients with cochlear-type hearing loss, Booth [26] found hyperlipidemia in 28% of the men and 10% of the women.
These authors observed hearing improvement of more than 10 dB in 9 of the 12 patients after antihyperlipidemic therapy. Sensory cochlear hair cells and vestibular receptors are especially affected by hypoxia, due to the terminal type of arterial circulation of the labyrinth.
In this manner, preventive measures may provide restorative support to the injured cochlea. We required all patients to rate their tinnitus from 1 to 10, with 10 being loudest (Table 1). Each level was defined by short explanations to simplify the patients' grading of their tinnitus. These suppositions are also stressed by the positive effect of the treatment with betahistine.

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